AKT1 and gastroesophageal reflux disease: However, aberrant PI3K/Akt activation may also drive pathological outcomes, such as glial cell proliferation and excessive inflammation, exacerbating stroke-induced tissue damage.[23,24] Collectively, these findings suggest that precision-targeted strategies modulating the PI3K-Akt pathway may provide novel avenues for investigating the shared pathogenic mechanisms of GERD and stroke, as well as developing dual-purpose therapeutic interventions.